Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isosorbide-5-mononitrate (IS-5-MN) is an active metabolite of isosorbide dinitrate with a longer plasma half life. Aim of the study was the evaluation of the effects of 40 mg/day of IS-5-MN on exercise capacity in patients with heart failure NYHA class II. After 1 week of wash-out, 10 patients with heart failure NYHA Class II, assumed 20 mg bid for 3 weeks. Bicycle ergometer tests were performed before (A), at the end of therapy (B), and 1 week later (C); in phase B the stress test was performed after 6 hours from the last assumption of IS-5-MN. We measured 24 hour urinary 6K-PGF1 alpha, the stable metabolite of prostacyclin, basal plasma renin activity (PRA) and plasma aldosterone, exercise-release of epinephrine and norepinephrine at the end of each phase of the study. The treatment with IS-5-MN improved the exercise capacity sigma (Watt.min), A less than (B = C), (p less than 0.01), while delta of heart rate (HR) during exercise (basal HR - maximal exercise HR)/(Watt.min), decreased, A greater than (B = C), (p less than 0.008). Basal BP and HR did not change. This fact seems consistent with the hypothesis of a combined effect of nitrates on both the venular and the arteriolar districts. Basal PRA and aldosterone, and catecholamine release during exercise after IS-5-MN did not change, while only norepinephrine increased 1 week after the end of the therapy, (A = B) less than C, (p less than 0.05): 24 hour urinary 6-K-PGF1 alpha increased after IS-5-MN A less than (B = C), (p less than 0.05). The results indicate that medium-term IS-5-MN treatment increases exercise capacity in patients with heart failure NYHA class II and that the effect lasts for 1 week after nitrate withdrawal at least. Prostacyclin is probably involved in medium-term clinical effect of IS-5-MN.
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PMID:[Effects of isosorbide-5-mononitrate on exercise capacity, prostacyclin synthesis, the renin-aldosterone axis and catecholamines in patients with cardiac insufficiency]. 275 47

Isosorbide-5-mononitrate was administered in a continuous intravenous infusion, according to the haemodynamic response, to 19 patients with left heart failure of ischaemic aetiology; 12 with acute heart failure complicating an acute myocardial infarction and 7 with chronic ischaemic failure. In both groups, the following statistically significant haemodynamic changes were observed: a decrease in PCWP from 25.4 +/- 4.6 to 17.2 +/- 4.6 mmHg; an increase in SWI from 19.1 +/- 10 to 23.6 +/- 13.1 gm m-2; a slight increase in cardiac index with no change in arterial pressure and only minimal decrease in vascular resistance. There were two major differences in the haemodynamic response between the patients with acute heart failure and those with chronic disease: (a) the duration of the effect of isosorbide-5-mononitrate on the PCWP was longer in the first group (mean, 8 hours, compared to 1.5 hours in the chronic group), and (b) the effect on afterload was more pronounced in the group with chronic ischaemic failure than in the first group. Thus, isosorbide-5-mononitrate administered by intravenous infusion under careful monitoring appears to have a beneficial role in the treatment of acute as well as chronic ischaemic heart failure.
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PMID:Haemodynamic effects of intravenous isosorbide-5-mononitrate in acute and chronic left heart failure of ischaemic aetiology. 340 14

Isosorbide-5-mononitrate is a longer acting active metabolite than the parent drug, isosorbide dinitrate (ISDN), with a half-life of around 4 hours. In coronary heart disease, myocardial infarction and in heart failure it causes a typical nitrate action on the central hemodynamics, but due to a complete systemic availability with high and predictable systemic drug levels, a drug action with a lower interindividual variability than with ISDN is to be expected. There is a close correlation between serum level and effect. The antianginal exercise tolerance increasing and unwanted effects as well as the development of tolerance to the drug action are comparable with those of ISDN. This naturally long-acting metabolite in ISDN works usually with a standard dosage of 20 mg twice daily.
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PMID:Oral isosorbide-5-mononitrate: pharmacokinetics and clinical efficacy. 355 38

Opiates and loop diuretics are the mainstay of treatment of acute pulmonary oedema, but it is now recognized that immediate response to intravenous loop diuretics is acute vasoconstriction with impaired cardiac performance. It therefore seemed appropriate to compare the effects of intravenous isosorbide 5-mononitrate and frusemide on systemic and coronary haemodynamics in a group of patients with chronic cardiac failure at cardiac catheterization. Intra-arterial blood pressure was recorded from the ascending aorta, pulmonary capillary wedge pressure and cardiac output were measured using a Swan-Ganz thermodilution catheter. Coronary venous blood flow was measured using a thermodilution technique and A-V oxygen difference across the myocardium was obtained from simultaneous blood sampling in the aorta and coronary sinus. Absolute myocardial nutrient blood flow was measured using a 133Xe clearance technique. Frusemide in a dosage of 0.5 mg/kg given intravenously provoked acute vasoconstriction with falls in cardiac output and stroke volume. Pulmonary capillary wedge pressure was unchanged in the first 60 min after administration of frusemide. Isosorbide 5-mononitrate in a dosage of 15 mg intravenously, significantly reduced the pulmonary capillary wedge pressure within 5 min, and with the subsequent fall in systolic arterial blood pressure, cardiac output was maintained. These results suggest that intravenous isosorbide 5-mononitrate could well be of value in the immediate management of the patient with acute pulmonary oedema.
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PMID:A comparison of intravenous elantan and frusemide in patients with chronic cardiac failure. 360 6

The objectives of this study were to determine the effects of low flow oxygen and isosorbide dinitrate on rest and exercise biventricular ejection fractions in patients with chronic obstructive pulmonary disease and to relate these ejection fraction responses to changes in pressure and flow. Nine patients with stable, moderate to severe chronic obstructive pulmonary disease who had no prior history of heart failure performed supine exercise with simultaneous hemodynamic and radionuclide ventriculographic monitoring. Eight patients performed a second exercise during low flow oxygen breathing and five performed a third exercise after ingesting 10 mg oral isosorbide. Oxygen led to a decrease in exercise pulmonary artery pressure in all subjects and a decline in total pulmonary resistance in five of the seven in whom it was measured. Right ventricular ejection fraction increased 0.05 or more only in subjects who had a decrease in total pulmonary resistance. Isosorbide fed to an increase in rest and exercise right and left ventricular ejection fractions with simultaneous decreases in pulmonary artery pressure, total pulmonary resistance, blood pressure and arterial oxygen tension. These results suggest that in patients with chronic obstructive pulmonary disease but without a history of right heart failure, the right ventricular systolic functional response to low flow oxygen and isosorbide at rest and exercise is, in part, determined by changes in total pulmonary resistance. The chronic relation between right ventricular ejection fraction and pulmonary hemodynamics in patients with chronic obstructive pulmonary disease remains to be evaluated.
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PMID:The acute effects of low flow oxygen and isosorbide dinitrate on left and right ventricular ejection fractions in chronic obstructive pulmonary disease. 688 28